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SBL (Skin, Blood, Lymph) Exam 1 and 2 > Chapter 25: The Skin > Flashcards

Chapter 25: The Skin Flashcards

1
Q

What are Macules (Patch), Papules (Nodule), and Vesicles (Bulla)?

A

Macules - flat lesion distinguished by surrounding color

  • macule < 5 mm
  • patch > 5mm

Papule - elevated dome or flat-topped lesion

  • papule < 5 mm
  • nodule > 5 mm

Vesicle - (blister); fluid filled, raised lesions

  • vesicle < 5mm
  • bulla > 5 mm
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2
Q

What is Acanthosis, Dyskeratosis, Hypergranulosis, and Hydropic Swelling?

A

A: diffuse epidermal HYPERplasia

D: abnormal keritinization BELOW the stratum granulosum

H: stratum granulosum HYPERplasia (rubbing)

HS: intracellular keratinocyte edema (viral infections)

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3
Q

What is Hyperkeratosis, Lentiginous, Papillomatosis, and Parakeratosis?

A

H: stratum corneum thickening

L: linear melanocyte proliferation within basal cell layer

P: surface elevation –> dermal papillae hyperplasia

PK: stratum corneum keratinization w/RETAINED NUCLEI (normal on mucus membranes)

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4
Q

What are the levels of the epidermis from superficial to deep?

A 
Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale

“Californians Love Gorillas in String Bikinis”

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5
Q

What is the Darier Sign, Stevens-Johnson Syndrome, and Auspitz Sign?

A

DS: dermal edema/wheal formation after rubbing lesion in mastocytosis

SJS: febrile form of erythema multiforme

AS: punctate bleeding in psoriasis when scale is lifted

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6
Q

What is the difference between Freckles, Cafe Au Lait spots, and Lentigo?

A

F: MOST COMMON pigmented lesion of childhood

  • appear AFTER sun exposure (norm. melanocytes)
  • focal melanin overproduction

CAL: seen in NEUROFIBROMATOSIS

  • larger than freckles; INDEPENDENT of sun exposure
  • aggregated melanosomes

L: benign, linear melanocytic hyperplasia

  • restricted to cell layer ABOVE basement membrane
  • do NOT darken with sun exposure
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7
Q

What is are Melanocytic Nevi and how are they generated?

A
  • pigmented moles caused by acquired mutations of RAS or BRAF; leads to period of proliferation that is turned OFF by P16/INK4a
  • rarely gives rise to melanoma, although melanomas have disrupted P16/INK4a inhibition
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8
Q

What is the difference between a Junctional, Compound, and Intradermal nervus?

A

J: nests of nevus cells at dermoepidermal junction

  • seen in kids
  • FLAT MOLE

C: nests/cords of melanocytes into DERMIS

  • looks like neurological tissue (BENIGN)
  • RAISED MOLE

I: complete loss of nests
- prominent during pregnancy

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9
Q

What is the difference between:

Black Nevus
Spindle/Epithelioid Cell Nevus
Halo Nevus
Dysplastic Nevus

A

BN: black-blue nodule (non-nested dermal infiltration)
- confused with MELANOMA

SCN: red-pink nodules; fusiform cells
- confused with HEMANGIOMA (common in kids)

HN: identical to acquired nevi but with lots of T-Cells
- lymphocytic infiltrate present

DN: coalescent intraepidermal nests; cyto ATYPIA
- potential precursor of MELANOMA

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10
Q

What is a Dysplastic Nevi and what mutation is associated with it? (Dysplastic Nevus Syndrome)

A
  • compound nevi with cytological/architectural atypia, lentiginous hyperplasia, and linear papillary dermal fibrosis (usually develop hundreds of dysplastic nevi)
  • usually flat macules that are > 5mm and LARGER than acquired nevi
  • AUTO DOMINANT mutation causes loss of CDKN2A (encodes p16/INK4a) = activated RAS/BRAF
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11
Q

What is the most deadly of all skin cancers? What type of radiation usually causes it?

A

MELANOMA

  • usually due to UV radiation (worst is UVB) exposure but also some from AUTO DOMINANT inheritance
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12
Q

What are the two most common areas for melanoma to arise in females and males?

A

F: back and legs
M: upper back

BANL - back, arms, neck, legs

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13
Q

What are 3 of the most common mutations that occur in Melanoma tumors?

A
  • inhibition of CDKN2A
  • activation of BRAF or KIT (usually KIT)
  • activation of TERT (telomerase)
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14
Q

What is the difference between Radial Growth and Vertical Growth of melanoma?

What is the Breslow Thickness Scale?

A

Radial: horizontal spread in epidermis/sup. dermis

  • unable to metastasize
  • 3 classes

Vertical: dermal invasion of cells lacking cellular maturation (has metastatic potential)

  • increases as the depth of penetration increases
  • BRESLOW THICKNESS

BTS: distance between granulosum layer to deepest intradermal tumor layer

  • < 1 mm of invasion = 95-100% 5 yr survival
  • > 4 mm of invasion = 37-50% 5 yr survival
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15
Q

What are the ABCDEs of Tumor Identification?

A 
A - asymmetry
B - borders (irregular or regular)
C - variegated color
D - increasing diameter (concern > 6mm, most at 10)
E - evolution (change over time)
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16
Q

What are the 3 classes of Radial Growth melanomas? (LM/SSM/AL)

A
  1. Lentigo Maligna
    • indolent, older men, BEST prognosis
  2. Superficial Spreading Melanoma
    • MOST COMMON of the subtypes
    • horizontal growth, stuck in radial phase for awhile
  3. Acral Lentiginous
    • usually on Black/Asian extremities (soles/palms)
    • due to C-Kit mutation (treat w/imantinib)
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17
Q

What is Seborrheic Keratoses, what mutation does it carry, and what sign is associated with it?

A
  • common/spontaneous/benign epidermal tumor of the trunk, extremities, head/neck
  • round, flat, coin-like waxy plaques (tan-brown and velvety)

Mutation: FGFR3 activating mutation

Sign: Leser-trelat Sign (inc. keratinocytes - inc. TGFa)

  • sudden appearance of multiple seborrheic keratoses
  • also paraneoplastic syndrome (think visceral cancer)
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18
Q

What is Acanthosis Nigricans, what mutation does it carry, and what is it commonly associated with?

A
  • thickened hyperpigmented skin w/velvety texture see in FLEXURAL areas
  • prominent rete ridges, basal hyperpigmentation, hyperkeratosis WITHOUT melanocyte hyperplasia
  • most are benign, but most common association is with OBESITY and DIABETES (IGFR-1 activates same pathway as FGFR3)

Mutations: familial (Auto Dominant: FGFR3) OR hyperinsulinemia (inc. IGFR1 signaling)

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19
Q

What are Fibroepithelial Polyps (SKIN TAGS), what do they look like, and what are they associated with?

A
  • common cutaneous legion and are mostly sporadic
  • soft, flesh-colored tumors attached by slender fibrovascular STALK (benign epidermis)
  • usually inconsequential but normally associated with DM, obesity, or intestinal polyposis (also inc. in number during pregnancy)
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20
Q

What is the difference between an Epithelial/Follicular Inculsion Cyst and and Adnexal (appendage) Tumor?

A

FIC: cystic expansion of epidermis/hair follicle

  • can lead to extensive/painful granuloma formation
  • STINKY (filled with keratinaceous material)

AT: nondescript, fleshy nodules or papules (BENIGN)

  • confused with CUTANEOUS CARCINOMA
  • primarily affect apocrine glands (scalp/axilla)
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21
Q

What is Actinic Keratosis, what is Actinic chelitis, and what can Actinic Keratosis progress to?

A
  • hyperkeratosis of sun damage leading to cutaneous horns (exuberant keratin production of face/arms/dorsum of hands)
  • exhibit Parakeratosis, atypical basal cells, intracellular bridges

AC = cutaneous horns of the lip

  • can progress to cutaneous squamous cell carcinoma
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22
Q

What is Squamous Cell Carcinoma, what causes it, and what 3 mutations can it have (T/R/N)

A
  • 2nd most common tumor of sun exposed skin, usually occurring in males with < 5% chance for LN metastasis
  • biggest risk factor is LIFETIME exposure to sun, usually developing from Actinic Keratosis (sun damage) but can also be caused by immunosuppression (HPV5/8)
    mutations: TP53 (inc. pyrimidine dimers and error prone repair), RAS and NOTCH signaling mutations
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23
Q

What is the difference between In Situ and Invasive Squamous Cell Carcinoma?

A

IS: well-demarcated, red, scaling plaques

ISSC: NODULAR, ranges from well differentiated to highly anaplastic with necrosis/ulceration

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24
Q

What is Xeroderma Pigmentosum?

A
  • auto recessive mutation of nucleotide excision repair of pyrimidine dimers
  • defective excision repair = error prone repair
  • usually seen in YOUNG pts with skin cancer
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25
Q

What is Basal Cell Carcinoma, what mutation does it have, and what does it look like?

A
  • most common invasive cancer and malignancy worldwide; slow growing and aggressive, but very RARELY metastasize
    mutation: PTCH LOF = uncontrolled Hedgehog signaling
  • has pearly papules with telangiectatic vessels; nodules extend deeply into dermis as islands/cords of basophilic cells with hyperchromatic nuclei (PALLISADING)
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26
Q

What is Nevoid Basal Cell Carcinoma Syndrome and what mutation does it have?

A
  • aka Basal Cell Nevus or Gorlin Syndrome, usually seen in those < 20 yo
  • autosomal dominant mutation –> PTCH LOF mutation causing transcription factor GLI1 = tumor growth
  • 1/3 have pyrimidine dimers
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27
Q

What are the 2 tumors of the Dermis? (FH/DP)

A

Fibrous Histiocytoma (dermatofibroma) = BENIGN

Dermatofibrosarcoma Protuberans = MALIGNANT

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28
Q

Fibrous Histiocytoma (Dermatofibroma)

What is it and what does it look like?

A
  • benign dermal neoplasms w/Factor XIIIa (+) dermal dendritic cells occurring on legs of young females
  • firm, brown/tan papules with spindle-like fibroblasts in a well-defined non-encapsulated mass
  • also see pseudoepitheliomatous hyperplasia (downward elongation of hyperpigmented rete ridges)
29
Q

Dermatofibrosarcoma Protuberans

What is it, what mutation is it associated with, and what does it look like (2)?

A
  • slow, locally aggressive primary fibrosarcoma of the skin
  • translocation of COL1A1 and PDGFb causing overexpression of PDGFb = autocrine loop growth
  • has storifrom pattern (closely packed fibroblasts arranged radially = PINWHEEL) and honeycomb pattern (extension into SubQ FAT)
30
Q

Mycosis Fungoides

What is it, what does it look like, and what two cells are hallmarks of it (SZC/PM)

A
  • homing CD4+ T helper cell lymphoma that can evolve to Sezary Syndrome (seeding of blood by malignant T cells = systemic)
  • scaly red-brown patches on the trunk with FUNGATING Nodules (confused with psoriasis)
  • Sezary Lutzner cells (malignant T cells with cerebriform nuclei) and Pautrier microabscesses (bandlike aggregates within superficial dermis)
31
Q

Mastocytosis

What is it, what mutation does it have, and how does it present?

A
  • increased number of MAST CELLS in the skin
    mutation: acquired KIT receptor tyrosine kinase activation = Mast Cell survival and growth
  • Urticaria pigmentosum (widely distributed round/oval nuclei with nonscaling papules and plaques), pink-tan-brown nodules that are pruritic or blistering

STAIN FOR MAST CELL TRYPTASE AND KIT

32
Q

What are the two most common signs of Mastocytosis? (DS/Derm)

A
  1. Darier Sign - localized dermal edema and wheal on skin that is rubbed
  2. Dermatographism - dermal edema (beehive) occurring from localized stroking of normal skin with pointed instrument
33
Q

What is Ichthyosis and what is X-linked Ichthyosis?

A
  • epidermal maturation disorder leading to keratin build-up that looks like FISH SCALES; presents around birth
  • due to defective desquamation (compacted stratum corneum buildup with loss of basket weave pattern)

X-Linked: loss of STEROID SULFATASE (normally removed proadhesive cholesterol sulfate)

34
Q

What are 3 Acute Inflammatory Dermatoses (U/AED/EM) and what are 3 Chronic Inflammatory Dermatoses (P/SD/LP)?

A

Acute: urticaria, acute eczematous dermatitis, erythema multiforme

Chronic: psoriasis, seborrheic dermatitis, lichen planus

35
Q

What is Urticaria and what does it look like?

A
  • localized mast cell degranulation leading to dermal microvascular hyperpermeability (WHEALS)
  • develops within 24 hours normally
  • have sparse mononuclear infiltrates (edema and eosinophils) and widely spaced collagen bundles but NO EPIDERMIS CHANGE
36
Q

What is the difference between urticaria:

Mast Cell Dependent, IgE Dependent

Mast Cell Dependent, IgE Independent

Mast Cell Independent, IgE Independent

A

D/D - Type 1 localized hypersensitivity rxn due to Ag binding to mast cells via Fc receptors

D/ID - substances DIRECTLY cause mast cell degraulation (opiates, radiographic contrast)

ID/ID - local factors inc. permeability due to drugs

  • Hereditary Angioneurotic Edema
  • inherited deficiency in C1 esterase inhibitor
37
Q

Acute Eczematous Dermatitis

What is it, what causes it, and what does it look like?

A
  • primary irritant dermatitis (either inside or outside) that can be blocked w/steroids (palliatative; cure by removing offending agent)
  • due to T-CELL mediated (Type IV Hypersensitivity); Langerhans presents neoantigens to naive T-Cells, causing erythema/pruritis on re-exposure
  • red, papulovesicular, oozing, crusted lesions (prone to bacterial superinfection = YELLOW CRUST)
38
Q

In a pt. with Acute Eczematous Dermatitis, how can you tell the difference between Drug-related vs Contact-related causes?

A

D: lymphocytic infiltrate and eosinophils
- in deep/superficial dermal vessels

C: mononuclear inflammatory rxn
- superficial dermal layer

39
Q

What condition characterizes Acute Eczematous Dermatitis and what does it look like?

A

SPONGIOSIS

  • edema seeps into intracellular spaces of epidermis, splaying keratinocytes in STRATUM SPINOSUM and leading to intraepidermal vesicles
40
Q

Erythema Multiforme

What is it, what two conditions is it characterized by (SJS/TEN), and what does it look like?

A
  • self-limited Type IV Hypersensitivity caused by CD8+ T-Cells causing keratinocyte injury (CD8+ in central lesion, CD4+/Langerhans in peripheral lesion)
  • Stevens-Johnson Syndrome and Toxic Epidermal Necrosis (diffuse necrosis /sloughing of cutaneous/mucosal epithelium - burn pts)
  • has TARGETOID LESIONS (red, maculopapular with central pallor - necrosis of keratinocytes)
41
Q

What is Stevens-Johnson Syndrome?

A
  • severe, febrile form of Erythema Multiforme associated with extensive skin involvement
  • typically in children
  • erosion/hemorrhagic crusting of skin/lips and can cause bacterial superinfection
42
Q

Psoriasis

What is it, what is it caused by, and what does it look like?

What phenomenon are associated with it? (KP/AS)

A
  • chronic inflammatory dermatosis with autoimmune basis
  • associated with HLA-C gene (Th17/CD4/CD8 in skin)
  • lesions are SALMON colored plaques with loose SILVER-WHITE scales; causes “test-tube rack” rete ridges and thinned stratum granulosum (parakeratotic scaling)

P: Koebner Phenomenon: lesion appear due to trauma
- Auspitz Sign: bleeding when scales are removed

43
Q

Psoriasis

Where are spongiotic foci of neutrophils seen? (2)

A
  1. Stratum Spinosum = spongiform pustules

2. Stratum Corneum = Munro microabscesses

44
Q

Seborrheic Dermatitis

What is it, what is its most common presenting lesion, and what does it look like?

A
  • more common that psoriasis; inflammation of EPIDERMIS (involves areas with high lvls of sebaceous glands)
  • DANDRUFF is most common scalp lesion (others are papules/macules on yellow, greasy base)
  • causes Follicular Lipping (parakeratosis and acute inflammatory cells around HAIR FOLLICLES)
    • perivascular infiltrate of neutrophiles/lymphocytes
45
Q

What are the 6 P’s of Lichen Planus?

A

pruritic, purple, polygonal, planar, papules, plaques

46
Q

Lichen Planus

What is it, what do its lesions look like (WS/WL), and what does it look like morphologically (CB/ST)?

A
  • self-limited and resolves 1-2 yrs after onset; can cause squamous cell carcinoma; Koebner phenomenon

L: Wickham Striae (white dots or lines highlight the papules) and oral lesions are White and Lacy

M: Colloid/Civatte Bodies (necrotic basal cells in inflamed papillary dermis) and Saw Tooth Rete (lymphocytic infiltrate along dermal-epidermal border)

47
Q

What are 3 Inflammatory (P/BP/DH) and 2 Non-Inflammatory (EB/P) Blistering Disease?

A

IN: pemphigus, bullous pempigold, dermatitis herpetiformis

NIN: epidermolysis bullosa, porphyria

48
Q

Pemphigus

What is it, what causes it, and what does it look like?

A
  • inflammatory blistering due to autoantibodies leading to dissolution of intracellular attachments (tend to rupture)
  • caused by IgG Abs against DESMOGLEINS 1/2
  • causes acantholysis (dissolution of intracellular bridges connecting squamous epithelial cells) –> unmooring of keratinocytes
49
Q

What is the difference in appearance between:

Pemphigus Vulgaris
Pemphigus Vegetans
Pemphigus Foliaceus

A

PVu: MOST COMMON

  • muscosa, face/scalp/axilla/groin/trunk/pressure points
  • superficial vesicles that rupture easily
  • suprabasilar blister (“row of tombstones”)

PVe: large, moist, verrucous (wart-like) vegetating plaques with pustules (NOT blisters)

  • acantholysis immediately above basal layer
  • also epidermal hyperplasia

PF: benign/mild –> RARELY affects mucus membranes
- blisters in superficial epidermis at stratum granulosum

50
Q

How can you tell bullous pemphigoid apart from pemphigus based on morphology?

A

BP: subepidermal, non-acantholytic blisters

P: epidermal, acantholytic blisters

51
Q

Bullous Pemphigoid

What is it, what causes it, and what does it look like?

A
  • autoimmune blistering that tend NOT to rupture and are commonly found in elderly pts (skin/mucosa)
  • caused by autoantibodies to BPAGs that adhere keratinocytes to basement membrane (hemidesmosomes)
  • 2-8 cm bullae with clear liquid at the subepidermal levels w/linear dermoepidermal junction staining for Ig and complement; see degranulated EOSINOPHILS and inflammatory cell INFILTRATE
52
Q

Dermatitis Herpetiformis

What is it, what causes it, and what does it look like?

A
  • urticaria and grouped vesicles normally seen in males; associated with INTESTINAL CELIAC DISEASE
  • caused by autoantibodies (IgA) to dietary gluten that cross-react with reticulin (anchor fibrils keeping superficial dermis to basement membrane)
  • vesicles on extensor surfaces; Neutrophils/Fibrin accumulate at TIPS OF DERMAL PAPILLAE (micro-abcesses) and BASAL VACUOLIZATION above
53
Q

Epidermolysis Bullosa

What is it and what are its 3 types? (S/J/D)

A
  • group of NON-inflammatory disorders that blister due to PRESSURE, RUBBING, TRAUMA (inherited structural protein defects)
  1. Simplex Type (MOST COMMON)
    • Auto Dominant mutation of KERATIN 5 or 14
    • defects of basal cell layer (no keratin fibers made)
  2. Junctional Type
    • blistering at lamina lucida (otherwise normal skin)
    • Auto Recessive mutation of LAMININ subunits
    • normally binds hemidesmosomes/anchor filaments
  3. Dystrophic Type (SCARRING)
    • cutaneous blistering beneath lamina densa
    • Auto Dominant/Recessive
    • Type VII COLLAGEN mutation (COL7A1)
54
Q

Porphyria

What is it, what does it look like, and what is the Acute Intermittent subtype?

A
  • uncommon disturbance of porphyrin metabolism
  • urticaria and scarring exacerbated by sunlight, as well as vessel walls thickened by glassy serum proteins

AIP: painful abdomen, port-wine urine, psychological disturbances, polyneuropathy

55
Q

Acne Vulgaris

What is it, what two things cause it, and what does it look like?

A
  • in teen males due to keratinization of lower part of follicle –> forms keratin plug that blocks sebum release to skin
  • hypertrophy of sebacceous glands during puberty and Propionibacterium acnes (Gram + rod) that converts sebum into pro-inflammatory fatty acids
  • infiltrates of lymphocytes/macrophages are present and surround the follicle
56
Q

Acne Vulgaris

What is the difference between an Open Comedone and Closed Comedone

A

Open: small papule with central black keratin plug
- NON-INFLAMMATORY

Closed: follicular papules without visible central plug

  • plug trapped beneath the epidermal surface
  • INFLAMMATORY
57
Q

What is Acne Conglobata?

A
  • severe inflammatory acne resulting in sinus tract formation and dermal scarring
58
Q

Rosacea

What is it, what causes it, and what are its 4 stages?

A
  • nonspecific perifollicular lymphocyte infilitrate with dermal edema and telangiectasia in women
  • caused by high cutaneous lvls of CATHELICIDIN and activation of TLR2 –> upregulates kallikrein 5 in keratinocytes (alternatively process cathelicidin)
  • starts as flushing –> persistant erythema/telangiectasia –> neutrophils colonize follicles (granulomatous response) –> RHINOPHYMA (permanent thickening of nasal skin)
59
Q

What is Panniculitis and what are its two forms?

A
  • inflammation of SubQ adipose tissue, usually involving the lower legs
    forms: Erythema nodosum (most common) and erythema induratum
60
Q

Erythema Nodosum

What is it, what is it caused by, and what does it look like (early vs late)?

A
  • poorly defined; readily palpable but not well seen but become bruise-like and leave no scars while new lesions develop
  • caused by delayed Type IV Hypersensitivity to microbial or drug-related antigens (B-hemolytic strep, TB, sarcoidosis)
  • early (CT septae are widened by edema, neutrophil infiltration) then late (lymphocytic histiocytes, multinucleated giant cells, eosinophils –> septal fibrosis)
61
Q

What is a COMMON association with Erythema Nodosum?

A

SARCOIDOSIS –> non-necrotizing granulomatous IBO

62
Q

Erythema Induratum

What does it look like and who does it commonly affect?

A
  • affects adolescents and menopausal females
  • primary vasculitis of deep vessels supplying fat lobules of the subcutis (fat necrosis and inflammation)
  • typically occurs w/o underlying disease; erythematous, slightly tender nodules that ulcerate
63
Q

Verrucae (Warts)

What are they, what are they associated with (5), and what do they look like?

A
  • squamoproliferative disorder due to HPV (mainly children and adolescents) that are transmitted by contact
  • HPV 6/11 = anogenital warts, HPV5/8 = epidermodysplasia verruciformis (squamous cell carcinoma), and HPV 16 = in situ squamous cell carcinoma of genitals (E6 proteins abolishing p53 BAD)
  • papillomatous epidermal hyperplasia and koilocytosis (cytoplasmic vacuolization of superficial epidermal layers)
64
Q

What is the difference between:

Verruca Vulgaris
Verruca Plana
Verruca Plantaris/Palmaris
Condyloma Acuminatum

A

VV: MOST COMMON wart (gray-white-tan)
- common on hands/periungal with pebble-like surface

VP: flat wart; elevated/smooth/tan
- face/dorsum of hands; smaller than Vulgaris

VPP: 1-2 cm diameter; rough/scaly lesions
- on soles and palms

CA: soft, tan, cauliflower-like masses
- seen in genital areas

65
Q

Molluscum Contagiosum

What is it, what do they look like, and how are they diagnosed? (GS)

A
  • common, self-limited viral skin infection due to POXVIRUS (brick-shaped with dumbbell DNA); spread via direct contact (children)
  • umbilicated PINK papules with molluscum bodies (large cytoplasmic inclusions in stratum granulosum and stratum corneum)
  • diagnose with GIEMSA STAIN –> see curd-like material with MOLLUSCUM BODIES
66
Q

Impetigo

What is it (SA), what causes it, and what does it look like?

A
  • superficial bacterial infection of exposed skin, usually due to STAPH AUREUS and NO DERMIS involvement (lesions heal without scarring)
  • blisters form due to bacterial toxin that cleaves DESMOGLEIN 1 (cell-cell adhesion in uppermost epidermal layer; Pemphigus has AutoAbs to it)
  • erythematous macule that can appear with “HONEY-COLORED CRUST” due to drying serum from lesions; also see neutrophil accumulation beneath stratum corneum (subcorneal pustule)
67
Q

What is the most common cause of Superficial Fungal Infections? How can they be identified? (PAS)

A

DERMATOPHYTES that grow in soil and on animals

  • stay confined to the Stratum Corneum
  • stain BRIGHT PINK/RED on PAS
68
Q

What is the difference between:

Tinea Capitis
Tinea Barbae
Tinea Corporis
Tinea Cruris
Tinea Pedis
Tinea Versicolor?
A

TCa: head and SCALP (hairless patches/mild erythema)
- occurs in children

TB: BEARD; infection of beard area of adult men

TCo: BODY; affects all ages, particularly children

TCr: common in INGUINAL area of obese men
- upper thigh as moist, red patches/scaly borders

TP: ATHLETES FOOT; localized to web spaces

  • most inflammation is related to superinfection (bact)
  • can spread to nails (Onychomycosis)

TV: UPPER TRUNK; due to MALASSEZIA FURFUR

  • yeast; group of macules of variable size
  • fine peripheral scales
69
Q

What are the genes and associations of:

Cowden Syndrome
Muir-Torre Syndrome

Neurofibromatosis I
Neurofibromatosis II

Xeroderma Pigmentosum

A

CS: PTEN; trichilemmomas, breast/endometrial carcinoma

MTS: MSH2/MLH1; DNA mismatch repair and sebacceous neoplasia

NF1: NF1/neurofibromin (negative RAS signaling)
NF2: NF2/merlin (integrates cytoskeletal signaling)

XP: XPA (AUTO RECESSIVE); nucleotide excision repair
- MELANOMA

SBL (Skin, Blood, Lymph) Exam 1 and 2 (22 decks)

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